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CARDIO > Cardiac Impulse > Flashcards

Cardiac Impulse Flashcards

1
Q

what type of rhythm does the heart exhibit

A

autorhythmicity (beats in absence of external stimuli)

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2
Q

where do cardiac impulses origionate

A

SAN

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3
Q

what do cells in the SAN exhibit

A

spontaneous pacemaker potential

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4
Q

define pacemaker potential

A

slowly depolarises the membrane to a threshold to generate an action potential
decreased K efflux
funny current: Na and K influx
Transient Ca influx via T-type Ca channels

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5
Q

how do action potentials spread

A

cell-to-cell conduction via gap junctions from SAN to AVN where the AP is delayed

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6
Q

what is the only point of electrical contact between the atria and ventricles

A

AVN

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7
Q

how does an electrical impulse spread from the AVN to the ventricles

A

via the bundle of his branches and the purkinje fibres and cell-to-cell conduction in ventricles

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8
Q

do action potentials in pacemaker cells differ from action potentials in myocytes

A

YES

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9
Q

what effect does the sympathetic NS have on the heart

A

POSITIVE CHRONOTROPIC EFFECT = increased HR

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10
Q

how does the sympathetic NS increase HR

A

increases slope of pacemaker potential and speeds up conduction through the AVN (by decreasing nodal delay)

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11
Q

what effect does the parasympathetic NS have on the heart

A

NEGATIVE CHRONOTROPIC EFFECT = decreases HR

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12
Q

how does the parasympathetic NS decrease HR

A

decreases the slope of pacemaker potential and slows conduction through AVN (increases nodal delay)

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13
Q

what dominates the heart rate under resting conditions

A

vagal tone: exerts a continuous influence to slow intrinsic HR

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14
Q

what is an ECG

A

a record of the depolarisation and repolarisation cycles of cardiac muscle

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15
Q

where is the SAN located

A

upper right atrium beside SVC

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16
Q

when the heart is controlled by the SAN what is this called

A

sinus rhythm

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17
Q

what happens during the rising (depolarisation) of an action potential in pacemaker cells

A

Due to activation of long lasting L-type Ca channels resulting in Ca influx

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18
Q

what happens during the falling phase (repolarisation) of an action potential in pacemaker cells

A

Inactivation of L-type Ca channels

activation of K channels causing K efflux

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19
Q

what neurotransmitter is responsible for sympathetic innervation of the heart and what is its receptor

A

noradrenaline

adrenoceptor B1

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20
Q

why does the parasympathetic NS have no effect on myocytes (only affects APs in SAN and AVN)

A

due to no vagal innervation on ventricles

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21
Q

what neurotransmitter is part of the parasympathetic nervous system and what is its receptor

A

acetylcholine

M2 muscarinic receptors

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22
Q

what drug can be used to treat bradycardia to speed up HR as It is a competitive inhibitor of acetylcholine

A

Atropine

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23
Q

what effect does noradrenaline have on pacemaker K efflux

A

decreases

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24
Q

what effect does noradrenaline have on Na and Ca influx

A

increases

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25
what effect does acetylcholine have on pacemaker cell K efflux
increases
26
what effect does acetylcholine have on pacemaker cell Ca and Na influx
decreases
27
what is the HR of a patient with bradycardia
< 60 bpm
28
what is the HR of a patient with tachycardia
> 100 bpm
29
what does the P wave represent
atrial depolarisation
30
what does the QRS complex represent
ventricular depolarisation (masks atrial repolarisation)
31
what does the T wave represent
Ventricular repolarisation
32
what does the PR interval show
largely AVN delay
33
what is the ST segment
ventricular systole
34
what is the TP interval
diastole
35
how are AVN cardiac cells specialised to their function
small diameter | slow conduction velocity
36
what is the resting membrane potential of cardiac myocytes
-90 mV
37
what causes rapid depolarisation of myocytes and what is the new membrane potential when excited
fast Na influx +20 mV Phase 0
38
how does the action potential graphs differ in ventricular cardiac myocytes to pacemaker cells
myocytes have a plateau phase | due to Ca influx through L-type Ca channels
39
what happens during depolarisation of cardiac myocytes
inactivation of Ca channels | activation of K channels = K efflux
40
what happens in phase 0 in ventricular myocyte APs
fast Na influx depolarisation Na channels rapidly deactivated at threshold to allow Na entry
41
what happens in phase 1 in ventricular myocyte APs
closure of Na channels and transient K efflux (different channels from K influx channels)
42
what happens in phase 2 in ventricular myocyte APs
Plateau: most important Balances of conductance: mainly Ca influx balanced by K efflux (Ca trigger Ca from sacroplasmic reticulum to be released) Ca influx by L-type channels membrane potential stays slightly +ve for prolonged steady period
43
what happens in phase 3 in ventricular myocyte APs
final repolarisation closure of Ca channels and K efflux caused by: Ikr, Its, Ik1 (Ik1 = late period of rapid depolarisation, dominant in phase 4)
44
what happens in phase 4 in ventricular myocyte APs
resting membrane potential drivel of K efflux Na/K ATPase active so conductance doesn't change inside and outside the cells
45
what cells show a fast ventricular response
atrial and ventricular myocytes
46
how do atrial and ventricular APs differ
in atrial APs there is no plateau, additional ultra rapid delayed rectifier outward K current Ikur that is absent from ventricular cells initiates final depolarisation more rapidly
47
what drug does Digoxin target
Na/K ATPase inhibitor causes depolarisation
48
what causes depolarisation in SAN and AVN
calcium dependant channels | no phase 1 and 2
49
what is phase 4 of an AP in the SAN
pacemaker potential increased inward flux of Ca and Na only depolarisation funny current: HCN channel
50
what do HCN channels of the funny current conduct
Na and K | switches on at positive potentials
51
where does the funny current take effect
end of phase 3
52
what are the 3 important conductance channels important in pacemaker potential
Ik: outward flux of K Ical: inward movement of Ca If: inward movement of Na causing depolarisation in response to hyperpolarisaton causing funny current
53
why is the slop of pacemaker potentials between action potentials so important
sets the intervals and sets HR
54
what happens during phase 0 of a SAN AP
upstroke opening of L-type Ca channels (NOT voltage activated Na channels)
55
what happens during phase 3 of SAN APs
gradual repolarisation due to opening of delayed rectifier K channels mediating Ik K channels active
56
what are action potentials affected by
``` drugs hormones ANS cardiac disease pH blood electrolyte abnormalities ```
57
what happens once noradrenaline has binded and activated B1 adrenoceptor
Gs protein a-subunit binds GTP to adenylyl cyclase
58
what effect does the Gs protein have on B1
stimulates B1 to increase SAN AP frequency and HR | increased p.p. slope
59
what enhances the pacemaker potential increased slope
If and Ical
60
what reduces the threshold for APs
sympathetic NS | enhanced by Ical
61
what is a positive inotropic response
increased contractility | increased phase 2 of myocyte AP, increased Ca infux
62
for any end diastolic pressure sympathetic stimulation contractility is higher/lower
higher
63
define contractility
force of cardiac muscle fibre at any differing degree of stretch
64
what is positive dromotropic response
increased conduction velocity in AVN by the sympathetic NS debut to enhanced If and Ical
65
the sympathetic NS increases automaticity what does this mean
tendency for non-nodal regions to acquire spontaneous activity
66
what is a Positive Lusitropic action
decreased duration of systole | increased uptake of Ca in sarcoplasmic retiulum
67
the sympathetic nervous system decreases/increases the activity of the NA/K ATP ase
increases | dépolarises cardiac muscle fibres
68
what long term effect does the sympathetic NS have on the heart
increases mass of cardiac muscle/cardiac hypertrophy
69
parasymthatics NS only acts on nodal/myocytes
nodal cells
70
what action does acetylcholine take when it activates M2
Gi protein | a-subunit inhibits adenylyl cyclase reducing cAMP
71
what is the role of the b/gamma subunit dimer when acetylcholine binds to M2
opens specific channels: G protein could inward rectifiers (GIRKs) in SAN
72
what happens when GIRKS open
K flows out causing hyperpolarisation
73
what channels reduce the negative chronotropic effect
If and Ical | Ical reduces AP threshold increase
74
where does the negative inotropic effect occur
decreased contractility | in atria only due to decreased in phase 2 of cardiac action potential and decreased Ca entry
75
what is the negative dromotropic effect
decreased conduction in AVN decreased activation on Ca channels and hyperpolarization via opening of GIRK AV cells become hyperpolariseed
76
what diseases can parasympathetic NS casue
arrhythmias in atria
77
what is the role of the vaxsalva manoever
activation of aortic baroreceptors to increase parasympathetic activity in the effect of atrial tachycardia/flutter/fibrillation to suppress conduction
78
what is the role of the funny current
modulates pacemaker potential by causing a depolarisation current mediated by channels activating hyperpolarixation and cAMP
79
what channels control the funny current
HCN
80
what drug is used to block HCN channels to decrease the pacemaker slope and decrease HR and is given in conditions where the heart isn't receiving enough oxygen
Ivabradine

CARDIO (14 decks)

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